Lifeboat Foundation

Junk DNA can occasionally spit out useful genes. Randomly?

Emerging data suggests the seemingly impossible — that mysterious new genes arise from “junk” DNA.

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A team at Temple University in Philadelphia used a combination of a DNA-snipping enzyme to eradicate the viral genome from the human cell.

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What would you say if I told you that aging happens not because of accumulation of stresses, but rather because of the intrinsic properties of the gene network of the organism? I’m guessing you’d be like: surprised .

So, here’s the deal. My biohacker friends led by Peter Fedichev and Sergey Filonov in collaboration with my old friend and the longevity record holder Robert Shmookler Reis published a very cool paper. They proposed a way to quantitatively describe the two types of aging – negligible senescence and normal aging. We all know that some animals just don’t care about time passing by. Their mortality doesn’t increase with age. Such negligibly senescent species include the notorious naked mole rat and a bunch of other critters like certain turtles and clams to name a few. So the paper explains what it is exactly that makes these animals age so slowly – it’s the stability of their gene networks.

What does network stability mean then? Well, it’s actually pretty straightforward – if the DNA repair mechanisms are very efficient and the connectivity of the network is low enough, then this network is stable. So, normally aging species, such as ourselves, have unstable networks. This is a major bummer by all means. But! There is a way to overcome this problem, according to the proposed math model.

Continue reading “Hacking Aging” »

THE genome is written in an alphabet of just four letters. Being able to read, study and compare DNA sequences for humans, and thousands of other species, has become routine. A new technology promises to make it possible to edit genetic information quickly and cheaply. This could correct terrible genetic defects that blight lives. It also heralds the distant prospect of parents building their children to order.

The technology is known as CRISPR-Cas9, or just CRISPR. It involves a piece of RNA, a chemical messenger, designed to target a section of DNA; and an enzyme, called a nuclease, that can snip unwanted genes out and paste new ones in. Other ways of editing DNA exist, but CRISPR holds the promise of doing so with unprecedented simplicity, speed and precision.

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Dr DePinho released a paper in 2012, this builds on previous papers and his theory of the “telomere-p53-PGC axis”. This is a big reason along with the work of Dr Michael Fossel I believe telomerase therapy is probably the best chance of radical life extension in the near future. This is one of a number of papers that implicate dysfunctional telomeres in a cascade that causes mitochondrial dysfunction and various other aging consequences.

ABSTRACT Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1α and PGC-1β, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1α expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1α and PGC-1β promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.

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Cancer researchers dream of the day they can force tumor cells to morph back to the normal cells they once were. Now, researchers on Mayo Clinic’s Florida campus have discovered a way to potentially reprogram cancer cells back to normalcy.

The finding, published in Nature Cell Biology, represents “an unexpected new biology that provides the code, the software for turning off cancer,” says the study’s senior investigator, Panos Anastasiadis, Ph.D., chair of the Department of Cancer Biology on Mayo Clinic’s Florida campus.

That code was unraveled by the discovery that adhesion proteins — the glue that keeps cells together — interact with the microprocessor, a key player in the production of molecules called microRNAs (miRNAs). The miRNAs orchestrate whole cellular programs by simultaneously regulating expression of a group of genes. The investigators found that when normal cells come in contact with each other, a specific subset of miRNAs suppresses genes that promote cell growth. However, when adhesion is disrupted in cancer cells, these miRNAs are misregulated and cells grow out of control. The investigators showed, in laboratory experiments, that restoring the normal miRNA levels in cancer cells can reverse that aberrant cell growth.

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Cancerous melanoma cells, shown with their cell bodies (green) and nuclei (blue), are nestled in tiny hollow lumens (tubes) within the cryogel (red) structure. (credits: Thomas Ferrante, Sidi A. Bencherif / Wyss Institute at Harvard University)

A new biologically inspired “injectable cryogel whole-cell cancer vaccine” combines patient-specific harvested cancer cells and immune-stimulating chemicals or biological molecules to help the body attack cancer. It has been developed by scientists at Harvard’s Wyss Institute and Dana-Farber Cancer Institute.

This new approach is simpler and more economical than other cancer cell transplantation therapies, which harvest tumor cells and then genetically engineer them to trigger immune responses once they are transplanted back into the patient’s body, the researchers say.

Continue reading “Anti-cancer vaccine uses patient’s own cancer cells to trigger immune responses” »

An interesting paper that uses ALA to shore up telomerase activity, loss of telomeres inhibition of P53 expression and mitochondrial dysfunction in one go. They use ALA (alpha lipoic acid) to induce PGC-1α in this case though PGC1-alpha seems to be a potential target for intervention as I understand that ALA is difficult to deliver to cells. In this case this involves the vascular system and atherosclerosis.

http://www.cell.com/cell-reports/abstract/S2211-1247(15)00825-6

Short telomeres and Mitochondrial dysfunction are increasingly implicated as being closely linked as this 2012 Dephino paper demonstrates in the aging heart:

Continue reading “PGC-1α Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases” »

Most cancer-busting strategies focus on removing cancerous cells. While this approach has proved extremely effective on many patients, most treatments have unpleasant side effects and there are many strains which prove extremely challenging to remove. An alternative model to this is to alter instead of remove — fixing cancerous behaviour by ‘reprogramming’ cells that go rogue; essentially swiss finishing school for cellular miscreants. A study published in Nature Cell Biology now provides hope that this tactic could in fact work in many cancers.

Researchers from Mayo Clinic’s Florida campus have found that adhesion proteins, which act like a glue sticking cells together, actually interact with a cell’s ‘microprocessor’. This processor creates molecules called miRNAs, which regulate multiple genes and essentially activate or de-activate different behavioural programs (like commands in computer programming). When healthy cells bump into a neighbour and begin to glue together, these adhesion proteins normally influence both cells — tuning down growth pathways. In cancer, the lab found this adhesion is perturbed; de-regulating miRNA production and enabling rampant growth. When scientists corrected these miRNA levels, the growth was arrested.

Continue reading “Can We Reprogram Cancer Cells Back To Normal?” »